The deterioration of uterine calcium transport capacity induced by aging is a common problem for late-laying period hens, causing decline in eggshell quality. This study aimed to investigate the effects and possible regulatory mechanisms of dietary puerarin (PU) on calcium transport and eggshell quality in aged hens. Two hundred eighty-eight Hubbard Efficiency Plus broiler breeder hens (50-week-old) were randomly allocated to three dietary treatments containing 0, 40, or 200 mg/kg puerarin (PU), with 8 replicates of 12 birds each, for an 8-week trial. The results demonstrated that dietary PU ameliorated the eggshell thickness and strength, which in turn reduced the broken egg rate (p < 0.05). Histological analysis showed that PU improved uterus morphology and increased epithelium height in the uterus (p < 0.05). Antioxidative capacity was significantly improved via upregulation of Nrf2, HO-1, and GPX1 mRNA expression in the uterus (p < 0.05), along with enhanced total antioxidant capacity (T-AOC) and glutathione peroxidase (GSH-PX) activity, and decreased levels of the oxidative stress marker malondialdehyde (MDA) (p < 0.05). Meanwhile, PU treatment reduced the apoptotic index of the uterus, followed by a significant decrease in expression of pro-apoptotic genes Caspase3 and BAX and the rate of BAX/BCL-2. Additionally, calcium content in serum and uterus, as well as the activity of Ca²⁺-ATPase in the duodenum and uterus, were increased by dietary PU (p < 0.05). The genes involved in calcium transport including ERα, KCNA1, CABP-28K, and OPN in the uterus were upregulated by PU supplementation (p < 0.05). The 16S rRNA gene sequencing revealed that dietary PU supplementation could reverse the age-related decline in the relative abundance of Bacteroidota within the uterus (p < 0.05). Overall, dietary PU can improve eggshell quality and calcium transport through enhanced antioxidative defenses and mitigation of age-related uterine degeneration.

The aim of the present study is to evaluate the impact of chromium (Cr) supplementation on glucose and lipid metabolism in breast muscle in broilers under heat stress. A total of 220 day-old broiler chicks were reared in cages. At 29 days old, 180 birds were randomly assigned to three treatments (0, 400, and 800 µg Cr/kg, as chromium picolinate) and transferred to climate chambers (31 ± 1 °C, 60 ± 7% humidity) for 14 days. Growth performance, carcass traits, serum biochemical indices, fasting glucose and insulin, homeostasis model assessment of insulin resistance (HOMA-IR), as well as muscle metabolomic profiles and gene expression related to energy and lipid metabolism were analyzed. The results showed that, compared with the heat stress group, the groups supplemented with 400 and 800 µg Cr/kg showed higher dry matter intake and average daily gain, breast muscle ratio, and lower feed conversion ratio and abdominal fat ratio; chickens supplemented with 400 and 800 µg Cr/kg showed significantly lower serum corticosterone (CORT), free fatty acids, and cholesterol levels compared with the heat stress (HS) group (p < 0.05). Fasting blood glucose and HOMA-IR were also significantly reduced, while fasting insulin was significantly increased in the Cr-supplemented groups (p < 0.05). Metabolomic analysis revealed that Cr supplementation regulated lipid and amino acid metabolism by altering key metabolites such as citric acid, L-glutamine, and L-proline, and modulating pathways including alanine, aspartate, and glutamate metabolism, and glycerophospholipid metabolism. Furthermore, Cr supplementation significantly upregulated the expression of Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1 α (PGC-1α), ATP Binding Cassette Subfamily A Member 1 (ABCA1), Peroxisome Proliferator-Activated Receptor α (PPARα), and ATP Binding Cassette Subfamily G Member 1 (ABCG1) in both the hepatic and muscle tissue. This paper suggested that chromium supplementation may enhance energy metabolism and lipid transport like the findings of our study suggested.

Summer high temperatures (27–38 °C, more than 7 days) readily induce heat stress in late-laying broiler breeders, which impedes offspring growth and development. This study aimed to provide a scientific basis for improving the offspring development of late-laying broiler breeders during summer. Six hundred fertilized eggs from 50-week-old LiFeng broiler breeders were divided into five treatment groups (non-injected, NaCl-injected, 6 mg/egg L-arginine-injected, 3.5 mg/egg L-methionine-injected, 8.4 mg/egg L-leucine-injected), with six replicates per group and 20 eggs per replicate. Embryos were incubated for 21 days and chicks raised for 21 days post-hatch. Methionine injection significantly enhanced hatchability (+5.8%), increased daily chick weight gain (+8.8%), reduced serum urea nitrogen (−53.13%), decreased inflammatory cytokine levels, elevated antioxidant enzyme activities, lowered malondialdehyde content (−47.99%), and suppressed expression of inflammatory and apoptotic pathway genes. The comprehensive effect of methionine was the best among the three amino acids when injected into chicken embryos. Methionine promoted protein synthesis, enhanced antioxidant and anti-inflammatory capacities, and consequently improved chick growth performance.

Accurate prediction of amino acid requirements in fast-growing broilers is crucial for cost-effective diet formulation and reducing nitrogen excretion to mitigate environmental impact. This study developed a dynamic model to predict standardized ileal digestible amino acid requirements throughout broiler growth using a factorial approach and the comparative slaughter technique, considering maintenance, growth, and gender factors. The model was based on an experiment were designed using 480 15-day-old Arbor Acres chickens randomly assigned to 10 groups. A linear equation was derived using established growth and protein deposition curves to calculate maintenance and growth coefficients. Models for five essential amino acids under different amino-acid-to-protein ratios were created (R² > 0.70). The model effectively estimated daily amino acid needs and specific time intervals. Comparisons with NRC (1994), BTPS (2011), and Arbor Acres manual (2018) showed higher predicted requirements for lysine, methionine, valine, and threonine than Arbor Acres (2018) and BTPS (2011), significantly exceeding NRC (1994). Arginine predictions aligned with BTPS in early stages, but were slightly lower in later stages. This supports the further development of dynamic amino acid models.

The aim of the present study is to evaluate the impact of chromium (Cr) supplementation on glucose and lipid metabolism in breast muscle in broilers under heat stress. A total of 220 one-day-old broiler chickens were reared in cages. At 29 days old, 180 birds were randomly assigned to three treatments (0, 400, and 800 µg Cr/kg, as chromium picolinate) and transferred to climate chambers (31 ± 1°C, 60 ± 7% humidity) for 14 days. The results showed that, compared with the heat stress group, the groups supplemented with 400 and 800 µg Cr/kg showed higher feed intake and average daily gain, breast muscle ratio, and lower feed conversion ratio and abdominal fat ratio; chickens supplemented with 400 and 800 µg Cr/kg showed significantly lower serum CORT, free fatty acids, and cholesterol levels compared with the heat stress (HS) group (P < 0.05). Fasting blood glucose and HOMA-IR were also significantly reduced, while fasting insulin was significantly increased in the Cr-supplemented groups (P < 0.05). Metabolomic analysis revealed that Cr supplementation regulated lipid and amino acid metabolism by altering key metabolites such as citric acid, L-glutamine, and L-proline, and modulating pathways including alanine, aspartate, and glutamate metabolism, and glycerophospholipid metabolism. Furthermore, Cr supplementation significantly upregulated the expression of PGC-1α, ABCA1, PPARα, and ABCG1 in both the hepatic and muscle tissue. This paper suggested that chromium supplementation may enhance energy metabolism and lipid transport by upregulating glucose and lipid metabolism genes, thereby mitigating heat stress-induced metabolic dysfunction and growth impairment.